H. pylori infection is associated with MALT lymphoma and gastric adenocarcinoma and CagA is thought to be involved in cancer development.[2] Phosphorylated CagA is able to interact with the SHP-2 tyrosine phosphatase, rendering it functionally active, triggering a host cell morphological change to a more motile phenotype known as the "hummingbird phenotype".[1] This phenotype mimics an effect produced by hepatocyte growth factor which may participate in various aspects of cancer, including metastasis.[2] CagA is also a highly antigenic protein that is associated with a prominent inflammatory response by eliciting interleukin-8 production.